期刊
DRUG DISCOVERY TODAY
卷 21, 期 1, 页码 38-47出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.drudis.2015.07.014
关键词
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资金
- National Cancer Institute of the National Institutes of Health [R01CA160685]
- American Cancer Society Research Scholar Grant [RSG-12-214-01 - CCG]
- National Cancer Institute Center Support Grant [P30 CA016056]
- NATIONAL CANCER INSTITUTE [R01CA160685, P30CA016056] Funding Source: NIH RePORTER
X-chromosome-linked inhibitor of apoptosis protein (XIAP) has an important regulatory role in programmed cell death by inhibiting the caspase cascade. Activation of XIAP-dependent signaling culminates into regulation of multiple cellular processes including apoptosis, innate immunity, epithelial-to-mesenchymal transition, cell migration, invasion, metastasis and differentiation. Although XIAP localizes to the cytosolic compartment, XIAP-mediated cellular signaling encompasses mitochondrial and post-mitochondrial levels. Recent findings demonstrate that XIAP also localizes to mitochondria and regulates mitochondria functions. XIAP acts upstream of mitochondrial cytochrome c release and modulates caspase-dependent apoptosis. The new function of XIAP has potential to enhance mitochondrial membrane permeabilization and other cellular functions controlling cytochrome c release. These findings could exploit the overexpression of XIAP in human tumors for therapeutic benefits.
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